Download ophth-notes - WordPress.com

http://www.enlightenme.org/knowledge-bank/cempaedia/eye-initial-assessment
The external eye
Hordeolum externum (stye)
o
o
o
o
infection/abscess of lash follicle – including Moll (sweat
glands) or Zeis (sebum glands).
Cause - usually staph
Point outwards causing a lot of inflam.
Mgmt- local Abx – fusidic acid
Hordeolum internum
o
o
o
o
Abscess/infection involving meibomian glands- or meibomian cyst
Point inwards into conjunctiva and cause much inflame.
CF- vision may be affected if corneal planus occurs.
Mgmt- incision and curettage under LA
P.M.- Chalazion is more rounded and would not have a yellow head.
Blepharitis
o
o
o
o
o
Lid inflam
Cause- stapy (bacterial form due to lid commensuals),
rosacea, sebbroheic dermatitis (as a result of meibomian
gland dysfunction)
CF- spread to lid margins, burning, itching and scales on
lashes; eye irritation, dryness (tear film dysfunction) &
stickiness.
O/E= conjunctivial injection (dilatation of bv)
Mgmt- wipe crust from eyelids, Tears Naturale, fusidic acid and doxy- adults and
erythro- children.
Pinguelcula
o
o
o
o
Degenerative vascular yellow/grey nodule on
either side of cornea in the conjunctiva
Ass- wind/sand blown environments, adult male,
increased hair and skin pigmentation and sun
related skin damage.
If inflamed – pingueltitis – ttt with topical steroids
If affecting the cornea – ptyregium - ttt- surgery
Entropian
o
o
o
o
Inversion of lower eyelid due to degenerative fascial muscles.
Rare <40years
Corneal abrasion as lashes point inwards
Mgmt- taping lower eyelid, botox or surgery
Ectropian
o
o
o
o
Eversion of lower eyelid,
Increased drainage of tears – dry eyes, eye irritation, watering and exposure keratitis
Ass- old age, facial palsy
Mgmt- gold plate in upper eyelid to enable closure of eyelid
Upper lid malposition
o
o
o
Can be due to globe hypetrophy/excess tissue (pseudoproptosis) or intrinsic levator weakness
(true proptosis).
Due to congential, mechanical (xanthalasama, odemal, upper lid tumour), endocrine
(hyperthyrodisim), CNS (3rd nerve palsy, Horners).
Congential ptosis corrected surgically.
Lagopthalmos
o
o
o
o
Inability/difficulty closing the eyelid over globe
Corneal ulcers and keratitis
Causes: exophthalmos, mechanical impairment of lid movement,
leprosy, paralysed orbicularis oculi,
Mgmt- lubrication with liquid paraffin oil. May require
tarsograpphy,
Dendritic ulcers/herpes simplex virus keratitis
o
o
o
o
o
N.B
Keratitis = inflame of cornea (Layers of cornea;
epithelium, bowmans, stroma, dua’s dechemet and
endothelim )
Causes by HSV, usually 1, remains dormant in
trigeminal ganglion until re-activated.
CF- photophoia and watering, pain, redness, blurred
vision (corneal inflammation).
Stain with fluroescien 1%
Mgmt – acyclovir 3% (x5 daily) with steroid (to
prevent corneal invasion, scarring and blindness)
HSV affects corneal epithelium whereas HZO affects stroma & anterior uvea.
N.B. Marginal keratitis – caused by hypersensitivity reaction to
endotoxins colonising lids leading to immune complex deposition in
peripheral cornea. CF=keratitis. O/E= multiple peripheral
subepithelial corneal infiltrates= separated from the limbus by a clear
zone. Mgmt=topical Abx & steroids
Eyelid tumours
Benigno
o
Skin papilloma, seborrehorc keratosises (basal cell papillomas)
Keratocanthoma
o
o
Pyogenic granulomata as a response to injury.
Congenital vascular naevi (port wine stains and strawberry naevi can include eyelids)
Malignant
Basal cell cx
o
o
o
Rodent ulcer, nodular lumps with pearly edges +/- pearly
telangiecstasia.
90% of malignant
Mgmt- mohs microsurgery
Squamous cell cx
o
o
o
Common in upper lid, increasing age and in women
Arise form meibomian gland, zeis glands
Mortality – 10%
Malignant melaona
o
WLE
Merkel cell cx
o
Violacous nodule, elderly, rapid growth
Kaposi sarcoma
o
AIDS- post-radio, purple nodule
Tears and lacrimation
Anatomy
o
o
o
o
o
Tears/lacrimal fluid made by lacrimal gland S/T
Lacrimal gland alone innervated by facial nerve as a reflex but produced by various other
structures; e.g. meibomian gland, lacrimal gland etc.
1.2ul/min produced with approx. 6uL within the eye at any time
Drainage occurs via S and I punctum, via ampulla, via canaculli, Valve of Rosenmuller
draining into lacrimal sac, before entering nasolacrimal duct in to the I turbinate.
Tears composed of IgA, contain lysozyme and B-lysin for antibacterials
Acute dacrosystistis
o
o
o
Inflam of lacirmal sac – M enlargement, may spread to
surrounding tissue (cellulitis) & result in systemic upset.
Mgmt- imm Abx
Comp- abscess formation
Chronic dacrosystitis
o
Middle aged/elderly.
o
o
o
o
Lacirmal sac distention, mucopus discharge +/- nasolacrimal duct block
TTT- infection
If NSD completely blocked – dacryocystorhinostomy (DCR)
Ass – squamous cell cx
Nasolacrimal duct non-canalization
o
o
By 1 yr- should be canalized if not requires probing under GA
CF – persistent watery eye & prone to attacks of conjunctivitis
Dry eyes syndrome (keratoconjunctivits sicca)
o
o
o
Problem due to reduced production (old age, Sjogren’s
syndrome), or excessive evaporation (post-exposure
keratitis) or mucin deficency in tears (stevens-johnson
syndrome, chemical burns, phemigoid, avitaminosis A)
I- schirmers test >15mm in 5min
Sx ttt- artificial tears
Excess lacrimation
o
Causes – emotion, corneal abrasion. Foreign body, entropian, conjunctivitis, acute glaucoma,
iritis.
Ephiphora
o
o
o
Normal volume but not drained to I meatus
Causes- ectropian, blocked drainage system (idiopathic/tumour)
TTT- DCR for NLD obstruction.
Orbital Swelling
o
o
Lesions in the bony orbit = proptosis (protrusion of orbit)
If excessive pressure= deviation of eyeball +/- diplopia
Orbital cellulitis-SOS
o
o
o
o
o
o
o
Causes; HIB, staph a, strep pyognes, strep pneumoniae
Spreads from paranasal sinus, esp post sinusitis, external
ocular, dental injury/infection
Typical CF- child, swelling (conjunctival injection),
inflam of orbit, fever and reduced eye mobility
Optic nerve affected=RAPD
I- Prompt CT
Mgmt- IV Abx cefuroxime +/-surgery (drainage of abscess)
Comp- blindness (optic nerve compression) & systemic (cavernous sinus thrombosis, abscess
meningitis)
o
N.B.
Ass- rhabdomyosarcoma
DDx- pre-septal cellulitis- only eyelid affected, no ocular involvement
Carotico-cavernosus fistula
o
o
o
o
o
o
Post rupture of carotid artery aneurysm, backflow of blood into
cavernous sinus
Causes; spontaneous, trauma (75%).
CF- engorgement of vessels, lid & conjunctiva oedema.
O/E exophthalmos may be pulsatile with loud bruit (heard as
buzzing) over eye +/- tinnitus
I- cerebral angiopathy
Mgmt- embolization or ligation
N.B. Carotid artery dissection – ALWAYS- CF=sudden onset of Horner’s (MAP= mipancoastosis,
anhydrosis & partial ptosis-Muller’s muscle) with headache, pain in the face, neck/jaw, X of
recurrent neck trauma= high proportion in young people. Urgent CT. Aneurysmal dilatation= mass
effect on sympathetic fibres=Horner’s syndrome. Mgmt= observation, anticoag, carotid artery
stenting/ligation.
Orbital tumour
o
o
o
o
o
o
o
1o neoplasia rare
3% orbital mets (breasts, lung, GI)
Children- unilateral proptosis = 1st sign of neuroblastoma
Nasopharyngeal tumours may invade orbit
Mucoceles and pyoceles pf ethmoid and frontal sinus.
DDx=Hyperthyroidism; Graves ( eye disease- 30%.
Autoimmine reaction to orbital antigens= infiltration= oedema. CF= proptosis, chemosis, &
conjunctivial injection (redness), lid retraction, lid lag, restrictive eye movments & diplopia)
Conjunctivial redness=propotosis & lid retraction=corneal exposure. If unttt= corneal
ulceration & compressive optic neuropathy. Inferior rectus most affected, then medial rectus
I-CT orbit
Opthalmic shingles (herpes zoster opthalmicus-HZO)
o
o
o
Accounts for 20% of HZO involvement >55% thoracic spinal
nerve involvement
>50% involves eyes , cornea; signs +/-iritis, >40% sectoral iris
atrophy
CF- pain and neuralgia in V1 Trigeminal, with blistering rash,
involving the eyelid, Hutchinson sign (nasociliary branch
invovled), headache, blurry vision
o
o
o
Comp if ImmunoComp- dissemination & post-herpetic neuralgia – chronic pain in the region
of rash that can be delibitating
Mgmt- Aciclovir x5/24hrs/7 days or famciclovir x1/24hrs/7days
Refer – if >3days redness & Hutchinson sign (tip of nose) for ddx of anterior uveitis.
Retinoblastoma
o
o
o
o
o
1/15000 cases. AD, hereditary version, RB gene located 13q14.
Common tumour among children
CF- loss of red reflex- leukocoria, strabismus.
Good prognosis but loss of vision in affected eye due to enucelation. Also chemo/radio.
Screen relatives
Eye movements and squints (strabismus, psudosquints (prominent epicanthic folds) tropia and
phoria)
Non-paralytic squints- due to lazy muscles
o
o
o
o
o
o
Start in childhood
I- corneal reflection and cover test (Gobin’s principle= evaluate all aspects of
strabisums)
Esotropia (convergent) – turned in
o Common in children
o No causes/ due to hypermetropia
Exotropia (divergent) – one eye turned out
o Occur in older children and often intermittent
Hypertropia – turned up
Hypotropia- turned down
o Mgmt- 3O’s- optical (1% cyclopentolate to relax and mydriasis for thorough
examination e.g. cataracts, macular scarring, retinonlastoma & provide spectacles)
orthoptic (cover good eye with patch), operation (resection and recession of rectus
muscles, botox)
Paralytic squints- due to paralyzed muscles
3rd nerve palsy
o
o
o
CF- down and out and out, ptosis (due to levator palpebral superiosis), proptosis, fixed and
dilated pupil, aniscoria (different-sized pupils)
Causes- PCAneurysm- unless proven otherwise/ microvascular ischaemia (DM, HTN)- will
spare pupil
Mgmt- refer to neurosurgery, but ischaemic 3rd palsy- resolves in 3mnths.
4th nerve palsy
o
o
CF- diplopia and unable to look down and out, ocular torticolii (tilted head).
Causes- trauma, diabetes, tumour & idiopathic
6th nerve palsy
o
o
o
o
CF- diplopia in horizontal plane and unable to look out
Causes- tumour (increasing IOP), trauma to base of skull, MS.
Mgmt- botox,
Pupils
Physiology
o
o
Light shown in on eye, travels along afferent CN2 (Optic nerve) to LGN (thalamus) on either
side.
From LGN, efferent travel via occulomotor nerve (CN3) to ciliary muscles to enable
dilatation via sympathetic or constriction via parasympathetic.
Afferent defects
o
o
o
o
RAPD on light swinging test aka Marcus Gunn pupil.
CF- on swinging test, affected eye shows consensual response but not direct response
therefore afferents affected. Constriction to accommodation still occurs
Pathway-light, optic nerve, pre-tectal nucleus of mid-brain- EWN – to both ciliary muscles
via oculomotor.
Causes- optic neuritis, optic atrophy, retinal disease
Efferent defects
o
o
3rd nerve- thus same as before
Causes- cavernous sinus lesion, superior orbital fissure syndrome (fracture of SOF ), diabetes
or PCA aneurysm.
Horner’s syndrome
o
o
o
o
Disruption of sympathetic fibres
CF=unilateral facial anhydrosis, partial ptosis and miosis
Congenital Horner’s – iris heterochromia
Causes- Pancoast tumour (subset of lung cancers- in pleural apex, affecting brachial plexus=
pain, in shoulder & ulnar nerve distribution or arm & hand, upper limb wasting, can affect
LEFT recurrent laryngeal=hoarse voice), MS, aortic aneurysm, mediastinal masses.
Holmes-Adie pupil
o
o
o
o
o
Def- infection affecting pogstganglionic of parasympathetic.
Initially unilateral then bilateral pupil dilatation with delayed response to near vision effectto
Typical – young woman, sudden blur of near vision, dilated pupil, slow to accommodation,
esp to light (looks unreactive unless >15min intense light)
I- Slit lamp= wormy movements of iris (iris streaming ), tonic pupil
Holmes-Adie syndrome= absent knee/ankle jerks, tonic pupils and low BP
Argyll-Roberton pupil
o
Causes- neurosyphyllis and DM-
o
o
CF= bilateral miosis, pupil irregularity (they are both small but different sizes) and no
response to light, but response to accommodation fast aka Prostitutes pupils accommodates
but does not react.
I- spongy iris, pupil dilates poorly (parasympathetic affected) and maybe ptosis.
Other causes of fixed dilated pupils
o
Mydriasis, trauma (blow out fracture)= acute rise in orbital pressure, can fracture thin Inferior
and medial walls= oedema, muscle entrapment & nerve damage=diplopia, acute glaucoma,
coning.
N.B
Ddx for diplopia= Ocular myositis (inflame disorder of 1/more EOMs, superior and
inferior mostly affected, CF=diplopia with pain (pronounced on muscle involved), diagnosis with
CT/MRI=muscle thickening, mgmt.=immunosuppression), MG (autoimmune neuromuscular –
autoantibodies to Ach, CF=ptosis (bilateral & variable increasing with fatigue) & diplopia, facial
& proximal muscle wasting, dysphagia & dysponoea. Ass=thymomas, I= Ach R antibody, antistriated muscle antibody & Tensilon test, ice pack placed for 2min improves ptosis. Mgmt= oral
anticholinesterase= pyridostigmine )
Iris
Sectorial Iris heterochromia
o
DDx- normal variant, herpes simplex opthalmicus, Waardenburg syndrome Type 1 – AD
(snhearing loss, pigmented abnormalities of hair and skin and dystopia canthorum (wide nasal
bridge))
Refraction
o
o
o
Dependent on eye ball length and medium
Cornea 2/3, iris 1/3
Normal eyeball length = ~2.5cm
Myopia
o
o
o
o
Short sightedness – due to large eyeball, therefore
focussing before hitting the retina, requiring concave
lenses.
Genetic 18P, 12Q; rarely born myopic, develops by 6,
settles at late teens, if it continues increases risk of
cataracts.
Environ- thought to do with increased exposure to close
range in early life and mRNA and [MMP]
Mgmt- glasses, contacts, LASIK. Eye tests every 6
months when young.
Pathological myopia
o
Rare <3%
o
o
>6doipoters even >20dipoters
Comp- secondary degeneration leading to retinal detachment, choroidoretianl atrophy and
macular bleeding.
Hypermetropia
o
o
Long sightedness due to short eyeball thus focusing beyond retina, n
eed convex lenses
CF- tiredness of gaze, convergent squints in children
N.B. Emmetropia = normal refractive power
N.B. Amblyopia= lazy eye – with no organic cause/ strabismus – if in children must be correct <6
Astigmatism
o
o
o
Distortion in horizontal/vertical planes due to asymmetry of curvature of cornea/lens
Can exist on its own + hypermetropia or + myopia
Mgmt= toric lenses
Presbyopia
o
o
o
Young lens are able to accommodate within 0.35sec
Ability decreases due to stiffness of lens by 40years and is complete by 60 years
Requires reading glasses.
VF defects
Assessment
o
o
o
o
Tests
o
o
o
Unilateral/Bilateral
Are borders clear
Vertical/horizontal plane
Acuity?
Amsler grid – central vision at 30cm, appears distorted (metamorphosia) if maculopathy
Finger confrontation
Hat-pin confrontation
Causes
o Ischemia (stroke, TIA, migraine)
o Tumour
o AV malformation
o Abscess
o Drugs
P.M. PITS- also craniopharyngioma affects optic chiasm Superiorly= inferior/lower
quadrant defect, whereas pituitary tumour affects optic chiasm Inferiorly= superior/upper
quadrant defect.
The red eye
Acute closed angle glaucoma
o
o
o
o
o
o
Aqueous humour produced by ciliary body and drained via canal of Schlemm.
Acute closed- reduced drainage due to blockage,
raised pressure=ischemia= corneal, iris & retina
CF= red painful eye, corneal haze/glare (corneal
oedema), fixed & dilated pupil, IOP increases
form 15-20mmHg to >40mmHg, n&v (abdo pain),
reduced vision, corneal oedema (Must be reduced
<4hrs to prevent irreversible visual damage)
O/E- close both eyes, the one affected is tender & harder
Typical- middle aged, night time or dark room, dilated pupil, >40, female & hypermetropic
Mgmt- analgesia & antiemetics, pilocarpine (2-4%), timolol-non-selective beta blocker
(topically), acetazolomid (carbonic anhydrase inhibitor 500mg IV- due to N&V), mannitol
and finally peripheral iridectomy (at 12o’clock position in both eyes-so that eyelid covers
defect in iris & prevents scattering of light)
Anterior uveitis (acute iritits)
o
o
o
Uvea= ciliary body, choroid and iris thus anterior refers to inflame of ciliary body and iris
Ass= AS, sarcoidosis, IBD, Behcet’s, reactive arthirits &
ocular trauma.
CF= acute pain, photophobia, acuity decreased, normal
pressure, blurred vision, small pupil initially then
irregular or dilates due to adhesions (synechiae)
o
o
o
o
o/e=redness around limbus(ciliary flush)
I- Talbots test- pain on finger confrontation & slit lamp= white ppt (floating infalm cells &
flare-protein exudates), sometimes sterile (hyopyon)
Mgmt- cycloepentolate (topical mydriatic- relieve ocular pain) to prevent synechaie
(adhesions) and ttt with prednisolone every 2hrs to reduce inflam.
Comp=cataracts & 2o glaucoma
N.B- Posterior uveitis- minimal pain, photophobia but mainly complain of visual blurring & floaters.
N.B. Systemic investigations- if bilateral, granulomatous or recurrent.
Conjunctivitis
o
o
o
Causes; bacterial (purulent
discharge),viral (infectious adenovirus
& prodrome= sore throat, low-grade
fecer & myalgia) or allergic
(giant/cobblestone papillae).
CF- bilateral with discharge, red,
hyperamic vessels that can be moved
over sclera. Acuity NOT affected.
Eyes burn, itch & lacrimate. Discharge can
stick lids together
TTT – bacterial – chloramphenicol
(topical broad spectrum), allergicantihistamines (emedastine)
N.B
Neonatal conjunctivitis/ophtlamia
neonatarum – 1st 28days of life. CF=bilateral
discharge & eyelid oedema
Corneal abrasion
o
o
o
o
Breach of epithelium, occurs without keratitis, e.g. trauma
CF=pain, photophobia, blurred vision
I- fluroresein 1% (orange drops turn green on blue dye if epithelial breach )
Ttt- chloramphenicol
N.B. Penetrating eye injury= early closure of corneoscleral laceration with Abx as delay=
endopthalmitis which if severe=blindness.
Corneal ulceration
o
o
Causes; bacterial, fungal or viral or from vasculitis
Mgmt- gentamicin & cefuroxime/ ofloxacin but do corneal scrape and mc& s for blood agar
and chocolate agar (Haemophilus B & N. menin) and liaise with microbiology.
N.B. Bacterial keratitis- S.aures, Strep & pseudomonas. But N.gonorr, one of the few that can
penetrate corneal epithelium. Predisposing; contact lenses, trauma, blepharitis &
immunosuppressant. Bacterial keratitis=permanent corneal scarring, corneal thinning & perf,
mgmt=corneal grafting.
Episcleritis
o
o
o
o
o
o
Inflam below conjunctiva – inflam nodule
More common than scleritis but not as painful/or life threatening
Blood vessels engorged look blue (segmental hyperemia) & are
movable.
CF= aches, tender, acuity ok
Ass=RF, PAN/SLE
Mgmt- topical vasoconstrictors (phenylephrine), but usually self-limiting
NOT
Scleritis
o
o
o
o
o
SOS50% - bilateral, middle-aged women
CF=v. painful and engorged bv (entire sclera), oedema of
conjunctiva with scleral thinning (risk of perf), acuity rarely
affected
Ass- connective tissue disorders (RA) & HZO
Mgmt-oral NSAIDS but if severe; topical& `systemic
corticosteroids or immunosuppressive.
Subconjunctivial haemorrhage
o
o
Self-limiting but alarming
I- BP check
Sudden PAINLESS loss of vision
Questions
o
o
o
o
Onset <6hrs requires imm ttt
Headaches
Pain on eye movements
Co-morbidities – control
Anterior ischemic optic neuropathy
o
I- fundscopy shows pale/swollen optic disc
o Arteritic
o 5-10%
o Optic nerve damage due to posterior ciliary artery blockage (inflammation,
atheroma or emboli, e.g. GCA(medium to large sized arteries))
o Due to thromboembolism in artery
o CF- malaise, jaw claudication, pulseless temporal
artery, tender scalp/unilateral headache & neck pain
o N.B. systemic signs; fever, myalgia, malaise, reduced
appetite and loss of weight
o I- ESR and CRP increases, temporal artery biopsy
o o/e= swollen disc & flame hameorrages
o
o Mgmt- prednisolone to stop blindness, may require up to a year.
Non-arteritic- Atherosclerosis
o 90-95%
o Causes- DM, HTN, increase in lipids and smoking.
o Modify factors to prevent other eye being affected
o Histology=necrosis & apoptosis at level of photoreceptors
Vitreous haemorrhage
o
o
o
o
o
Leakage of blood from retinal vessels, new vessels (diabetic
proliferative retinopathy), branch, central retinal vein/artery, retinal
tear, retinal detachment, trauma etc
Comps- retinal detachment
CF if small= floaters/spots if moderate= red dots/no red reflex
I- B-US helps exclude retinal detachment.
Mgmt- spontaneously absorbed, might require vitrectomy if
large. In DM- wait 3mnths post photo-coag.
Posterior vitreous
detachment
Retinal detachment
Dense shadow that
Flashes of light
starts peripherally
(photopsia) - in the progresses towards the
peripheral field of central vision
vision
A veil or curtain over
Floaters, often on
the field of vision
the temporal side of Straight lines appear
the central vision
curved
Central visual loss
Vitreous
haemorrhage
Large bleeds cause
sudden visual loss
Moderate bleeds may
be described as
numerous dark spots
Small bleeds may
cause floaters
Subacute loss of vision- optic neuritis
o
o
o
o
o
o
Unilateral loss of acuity, can take hours or days
CF- RAPD, red desaturation, pain on eye moments (In RBN, optic
nerve sheath compresses the optic nerve), also central scotoma.
CF= 60%-normal, swollen- 23%, 18%-hyperaemia & blurred with
peripapillary haemorrhages -2%.
Recovery over 2-6wks - 45-80% will have MS <15years
Mgmt- methylprednisolone for 3 days followed by oral corticosteroid
for 11 days might delay LT disability
Other causes- neurospyhillis, other demyelination, Leber’s optic atrophy, diabetes and
vitamin deficiency, viral infections, vasculitis
N.B
Optic papilitis if optic head is affected & retrobulbarneuritis (RBN) if optic nerve affected
posteriorly. In RBN- acute stage looks unaffected, with optic atrophy occurring mnths later, in
papillitis – optic disc swelling.
N.B. Papilledema= bilateral optic disc swelling = blurring of the optic disc margins & venous
engorgement.
Transient loss of vision
o
o
o
o
Ischaemic (stroke, migraine, TIA)
MS
Subacute glaucoma
Papilloedema.
Central retinal artery occlusion
o
o
o
o
o
Not as common as CRVO; can affect central/branch
Thromboembolic cause; check BP, DM, HTN, (CVD-carotid and valves)
CF= CF-90%, RAPD(sec)
I- pale fundus, cherry red spot
Mgmt- <90minutes =required increasing blood flow to retina, ocular
massage, removed aq fluid from anterior chamber (paracentesis) and
anti-HTN agents/LT-antiplatelet therapy/carotid
endarterectomy.
Central retinal vein occlusion
o
o
o
o
o
o
o
Increases with age and is more common than
CRAO
CF=CF
I- Fundoscopy- tortuous dilated vessels, optic
nerve swelling (papilloedema) and retinal
haemorrhages (diffuse flame shaped1)
RF- DM, HTN, old age raised IOP, smoking &
lipids.
Types; ischemic (cotton wool, RAPD-if severe
case) and non- ischemic
LT outcome form 6 months to 1 year; macular
oedema and iris neovacualrisation (IRIS
RUBREOSIS) = <100 day neovascular glaucoma (RUBREOTIC GLAUCOMA).
TTT of neovascular glaucoma – aggressive pan-retinal laser photocoagulation/intravitreal
injection of anti-VEGF
Branch retinal vein occlusion
o
o
o
o
o
Unilateral vision loss,
Retinal ischaemia leads to VEGF
TTT of neovascularisations - photocoagulation
TTT of macular oedema- grid pattern argon laser photocoagulation (+/arterial crimping)
o/e= produces haemporrgahe & vessel tortuosity & corresponds with VF
Gradual loss of vision
Charles Bonnet syndrome
o
Visual hallucination, elderly, with gradual loss of vision
Chroiditis (choroidoretinitis)
o
o
o
o
o
Inflam of choroid by orgs leading to granulomatous appearance
Toxocara, toxoplasmosis>sarcoidosis and TB
I- CXR, Mantoux test, serology
Mgmt- dependent on orgs
Acute phase- blurred vision, grey/white raised patch, vitreous
opacities and cells in A chamber & Late phase- choroid retinal scar
Choroid melanoma
o
o
o
Common malignant tumour
Grey/black mottled appearance with haematogenous spread or
orbital spread/raised brown fundal mass
Mgmt- enucleation, irradiation, photocoagulation, microsurgical
resection.
Age related macular degeneration
o
o
o
o
o
o
Chief cause of blindness in UK
Elderly affecting central vision
Types; Wet (chroroidal new vessels, showing fluid
exudation) and Dry (drusen and degeneration at
macular, usually both eyes affected, atrophy &
retinal pigment epithelial changes)
Mgmt WET > DRY. Wet- photodynamic therapy,
laser and intravitreal anti-VEGF.
Wet has the worst prognosis.
Advise to quit smoking and increase green veg
Optic atrophy
o
o
o
I- pale/swollen optic disc
Causes increase in IOP, Paget’s disease of skull, retinal damage,
ischemia
Causative; tobacco, methanol, lead, arsenic, quininine.
Optic nerve drusen
o
o
Abnormal metabolism leads to build up calcium in
mitochondria, exudation = calcified mitochondria
I- optic disc irregular, lumpy yellow matter, no optic cup
and abnormal branching patterns of vessels.
Chronic simple (open angle) glaucoma
o
o
o
o
o
Asx until VF affected, as central vision intact therefore late presentation and irreversible optic
nerve atrophy
>21mmHg requires yearly screen = optic disc cupping, nerve damage, scotomata near blind
spot.
Nasal and Superior fields are lost first (temporal last)
>0/4 cup to disc=glaucoma.
Fundsocpy= pale optic discs (atrophy), cup widens and deepens, so blood vessels appear to
have breaks as they disappear into the cup(sharp turning=bayoneting)
RF
o
>35, (+)ve Fx, Black, myopia, diabetic/thyroid eye disease. – raised IOP, only indicator of
pressure thus lowering prevents glaucoma.
Tests
o
o
o
VF screening
Optic disc ratio/cupping – 0.4-0.7, >0.9=severe
IOP
Drug ttt- reduce IOP by 30% baseline
o
o
o
o
o
o
Prostaglandin analogues (latonprost)- increase uvealscleral drainage SE: long eye lashes,
changes to pigmentation of iris and around eye, pruritus and irritation
B blocker- timolol – decrease production of aqueous. SE- dry eyes, low exercise tolerance,
allergy. CI- asthmatics and heart failure
A-adrenergic blockers- brimonidine- increase drainage and decrease production of aq
humour. SE-lethargy & dry mouth.
Miotics- pilocarpine- increase aq flow drainage SE-miosis, brow ache and reduced acuity.
Carbonic anhydrase inhibitors- acetazolamide – decrease production of aq humour. SE:
dyspepsia, low K+, paraesthesia. CI-pregnancy.
Sympathomimetics- dipivefrine – CI heart disease, high BP & closed angled glaucoma. SE,
red eyes/low vision, sore.
Surgery if drug ttt fail
o
o
o
Trabeculectomy- to increase drainage into a conjunctival bleb.
Comp= early failuire, hypotony, bleb leakage, infection
Argon laser trabeculoplasty- short-term.
Cataracts
o
o
o
o
o
Measure fasting bm
Worldwide top cause of blindness, then vitamin
A def, trachoma and onchichoreisis.
Opacification of lens- leukoria if mature,
Can be congenital
>75% of >65 & 20% of 45-65 yr olds.
o
o
Avoid high oxidative stress e.g. smoking.
Different types;
o Christmas tree/dot (dystrophia myotonica),
o nuclear cataracts (old age)
o Corticol/spoke like/wedge (old age)
o Anterior and Posterior pole (localized and inherited, lie in visual axis)
o Subcapsular (steroid use & deep to lens capsule )
o
blurred vision, gradual vision loss +/- frequent spectacle changes, dazzling in bright lights
and may cause mononuclear diplopia. Children- squint, loss of binocular function, leukoloria,
nystagmus. Pinhole can improve visual acuity, as blurred vision due to refractive error
CF
Surgery
o
o
o
o
o
o
o
o
Temp relief- mydriatic drops, sunshades but if affection lifestyle & cannot read 67 feet for
driving then surgery.
Risk of surgery- 2% serious
Day case under LA- involves small slit at limbus, phaecoemulsification (broken by US) of
lens contents (via cannula), placement of artificial lens capsule (foldable).
P lens remains and can thicken, 5-30% opacifies= return of cataract, a small hole is made
using a YAG laser.
Comp= A uveitis, retinal detachment, VH, glaucoma = permanent visual loss. Post-op
bacterial endopthalmitis- rare comp- proptosis & restriction of eye movement 2o to
enlargement of EOM (cf=poor vision, pain & significant inflammation <2wks of surgery.
Fundoscopy= obscured by vitritis)
After phaeco- normal activities can assume the following day
Abx & anti-inflam drops for 3-6weeks post-op.
Comps- P lens rupture, dry/gritty eyes (Viscotears)
The retina
o
o
Consists of 2 layers; neurosensori retina and pigmented retina.
Macular 5mm, contains fovea, fovea centralis- high concentration of cones – for visual acuity
Optic disc
o
Note colour(pink), cup (0.4-0.7) and contour (ovoid in astigmatism) & 2:3 A:V ratio.
Retinal detachments
o
o
o
P- rhegmentous – rhegma is a break in epithelium e.g. retina
tear leading to fluid accumulation that results in the separation
of retina (neurosensory from RPE= accumulation of vitreous
fluid in subretinal space), secondary to intraocular prob, post
cataract surgery. Increased risk in myopics – esp post cataract
surgery.
4 F’s= flashes (50%), floaters, field defects & fall in acuity
CF- curtain falling down (SUDDED PAINLESS), if superior falls down then inferior fields
lost, red eye reflex lost. If macula affected= no central vision.
o
o
o
I- ballooning, grey effect. On slit lamp= Shafer’s sign (floating pigment cells in the in A
vitreous)
Mgmt- vitrectomy, gas tamponade (silicon oil) silicon lens implant. Cryotherapy/laser coag
secures retina. Post-op re-detachment – 5-10%
Prognosis- if macular detachemed >24hrs = full recovery
unlikely.
Retinitis pigmentosa
o
o
o
o
Inherited, usually AR, but AD has best prognosis, X linked has
worst prognosis.
CF= Funnel (aka tunnel) vision, worse at night, at 20 some have <6/60 and by 50, some have
ability to read (25%).
O/E= black bone spicule-shaped pigmentation, mottling of retinal
pigment epithelium.
Ass; Refsum disease (cerebellar ataxia, peripheral neuropathy,
deafness, ichthyosis/fishy-scale), usher syndrome (SNHL), Alport
syndrome (different types)
Toxoplasma
o
o
Intracellular protozoan
I-bilateral punched out holes, heavily pigmented chorioretinal scars & if macular affected,
decrease in acuity.
Macula
Macular holes
o
o
Full thickness defect of retinal tissue, involving fovea = decreased acuity.
3/1000 >55yrs, 12% chance of other eye being affected
Presentation
o
o
Distorted vision with visual loss.
Tiny punched out area centre of macula – yellow white deposits at base
o
Slit lamp= semi-translucent area over hole= grey halo of detached retina
I
Causes
o
Idiopathic. Age-related shrinkage of perifoveal vitreous cortex, traction on fovea, detachment
and macula holes. Displacement of fovea- underlying xanthophyll pigment.
Stages
o
o
o
o
1=yellow spot at fovea; yellow donut
shaped ring. Vision usually good, 50%
progress to 2.
2=<400nm. Full thickness macula hole,
with cuff of subretinal fluid. Vision
reduced with image distortion.
3=>400nm, with localizd separation of
vitreous cortex.
4= complete hole with vitreous seperation
from entire macula and disc
Tests
o
o
o
Amsler grid
OCT
FA
Mgmt
o
o
o
o
o
Stage 1- wait and see may resolve spontaneously/
Vitrectomy, creating an air bubble (tamponade)- Pt lying on face 1-2 wks post-op. <95%
closure rates.
May require additional surgery
Comp= RD, iatrogenic retinal tears, enlargement of hole.
<2 years many develop cataracts.
The eye in DM
o
o
o
<150/85 will prevent DM retinopathy
Cause of blindness – 20-65
30% have ocular problems at presentation.
Structural
o
Diabetes accelerated glycsolication- increases sorbitol via aldose reductase – age-related
cataracts,
Patho
o
o
o
o
o
o
Micorangiopathy in capillaries, precapillary arterioles and venules cause occlusion +/leakage
Vascular occlusion leads to new vessels forming on choroid, retina, iris- VH =
proliferative DMR
New vessels are fibrous leading to traction- retinal detachment
Occlusion also causes cotton wool spots (ischaemic nerve fibres)
Vascular leakage- as pericytes are lost, capillaries bulge (micoraneurysms)
Oedema and hard exudates (lipoprotein & lipid filled macrophages)
o
Rupture of micro aneurysm – flame shaped haemorrhages – deep= blot haemorrhages.
Classification
o
o
o
o
Before; background, pre-proliferative and
proliferative +/- maculopathy
Now – non-proliferative diabetic retinopathy
classed as mild, moderate and severe, can become
sight threatening proliferative DMR
Proliferative DMR- fine new vessels appear on
optic dsic, retina =VH (more common in DM1,
50% blind in 5 years)
Maculopathy mapped; foveola, foveola centralis, parafoveal and perifoveal. Leakage from
vesssels= macular oedema & threaten vision. (More common in DM 2)
Traditional classification
New classification
Mild NPDR
Background retinopathy




microaneurysms (dots)
blot haemorrhages (<=3)
hard exudates
Pre-proliferative retinopathy





1 or more microaneurysm
Moderate NPDR




microaneurysms
blot haemorrhages
hard exudates
cotton wool spots, venous beading/looping and
intraretinal microvascular abnormalities
(IRMA) less severe than in severe NPDR
cotton wool spots (soft
exudates; ischaemic nerve
fibres)
> 3 blot haemorrhages
venous beading/looping
deep/dark cluster
Severe NPDR
haemorrhages
more common in Type I DM,
 blot haemorrhages and microaneurysms in 4
treat with laser
quadrants
photocoagulation
 venous beading in at least 2 quadrants
 IRMA in at least 1 quadrant
Treatment
o
o
o
Control of bm & treat co-morbidities
Photocoag by laser- treat maculopathy (grid/focal) and
proliferative retinopathy (panretinal)- scatter laser >1000
applications may require 2 sessions. N.B. Pan-retinal does not
improve vision, prevents blindness.
VH- viterectomy
Ocular palsies
o
o
Argyll-Roberstons & Horners (topical 4% cocaine will only dilate normal eye, due to cocaine
blocking the re-uptake of NA, in Horner’s, NA is not secreted thus no effect. Ddx= Pancoast
tumour of lung)
3rd & 6th
Tropical eye disease
Trachoma
o
o
o
Chlymydia trachomatis – one of the causes of
blindness
Spread by flies, related to cattle
Prevention- face washing & good
water/sanitation.
Staging
o
o
o
o
1- Lacrimation, follicles in the upper lid show
granular appearance
2-erythema, larger follicles and both lids
affected. Pannus of capillaries grow towards
cornea
3-scar tissue as follicles rupture & pannus
more advanced.
4- inversion of eyelid and irritation by
eyelashes. Cornea may ulcerate.
Mgmt
o
o
o
o
Mass anti-trachoma treatment – tetracycline 1% eye ointment 12hrly- for 5 days each month
for 6 months.
Active disease, tetracycline 250mg.6h po for 14 days & 8hrly for 6 weeks.
Single dose azithromycin in children is 78% effective in children.
Surgery- e.g. lid margin splitting + tarsal plate fracture +everting sutures
Onchioresiss/ river blindness
o
o
o
o
o
o
Microfilarea of namtode onchocero volvulus, transmitted by
black flies of Simulim species, 95% Africans affected
Unless eyes affected, most confined to skin
Fly bites =nodules which microfilarea released, invade
structures of eye,
Investigation- dead or swimming/ floating in Anterior
Microfilarea cause inflame, then fibrosis occurs around them, reaction causes cornal opacitis
(nummular keratitis )
Chronic iritis = synechia & may ppt cataracts, with iris becoming totally fixed.
Tests
o
Skin-snip tests, triple antigen serology, PCR.
Mgmt
o
Ivermecting- single dose every 6-12monts till adults die aka macroflirae (lympathic system)
Xeropthalmia & keratomalacia
o
o
o
o
o
o
o
o
o
Vitamin A deficiney, 2-5yrs.
Night blindness & dry conjunctivae
Cornea unwettable & loses transparency
Bitots spots (small grey plaques) raised from
interpalpebral conjunctivia
Vit A reverses changes
Early corneal xerosisi reversible.
Keratomalacia- softening of cornea, +/- perf and extrusion
of intraocular contents.
Mgmt- retinol palmitate or retinyl palmitiate
Avoid vit A in pregnancy.
Blindness and partial sight
Causes
o
o
o
o
o
o
o
Trachoma
Cataracts
Glaucoma
Keratomalacia
Onchooreciases.
DMR
Irreversible and in developed coutnries = age-related macular degeneration
The Law
o
o
Registrable <3/60 or >3/60 with reduced VF
Partially sighted = <6/60 or >6/60 with VF
Colour blindness
o
o
o
o
Red/green mostly sex linked 8 in males & 0.5 in females
Blue-yellow acquired, 1:1
Ischiara 16 plates
Monochromatism- due to born without cones, were all cones contain same visual pigment.
Drugs in the eye
o
Eye unable to retain drops, every 5 min between drops & hold 2hrly
Mydriatic
o
o
o
o
Tropicamide- every 3hrs
Cyclopentoalte- 24hrs- prevents syncheia, as it’s a cycloplegic
=blurred vision, don’t drive
Not to be used is acute close angle glaucoma
Miotics
o
o
Pilocarpine
= reduces acuity, parasympathetic sweating, brow ache due to ciliary spasm, flue-like
syndrome, sweating, urinary frequency, dyspepsia.
Local anaesthetics
o
o
Tetracaine – abolishes cornel reflex
In children- proxymetacaine (less stinging)
Steroids & NSAIDs
o
Increase IOP and may progress dendritic ulcer so beware
Iatrogenic eye disease
o
o
Glaucoma may be ppt by steroid use, some mydriatic and anti-cholinergics (e.g. antiparkinson’s and TCAs)
Ethambutol stains contact lenses and any visual SEs should be reported.
Contact lenses
o
o
o
o
o
o
o
o
o
o
80% wear cosmetic
Medical reasons to -12 in hypermetropia. >+10 in myopia & keratoconus (degenerative
condition with blurred vision the only symptom)
Hard lenses 8.5-9mm
Gas permeable – may mist up during the day
Soft- lenses – 4 wks then disposes
Toric- astigmatism
Extended wear lenses can be worn up to 4 months.
Hard lenses – 2 solution one for cleaning & one for storage
SE= corneal ulcers/abrasion, giant papillary change, to mucoprotein in lenses &
keratoconjunctivities
Mgmt of pseudomonas cornal ulcers- oflaxacin
Miscellaneous
CMV Retinitis


Affects immunocomp (e.g. post renal-ttt)
CF= yellow-white retinal necrosis & haemorrhage (pizza
pie)
Choroidal neovascularization


Greyish lesions beneath the macula
Leakage of bllodd/fluid= acute onset of central visual
loss due to photoreceptor damage.